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Implications of ADAM17 activation for hyperglycaemia, obesity and type 2 diabetes
In this review, we focus specifically on the role that the metalloproteinase, A Disintegrin and Metalloproteinase 17 [ADAM17] plays in the development and progression of the metabolic syndrome. There is a well-recognised link between the ADAM17 substrate tumour necrosis factor α (TNF-α) and obesity,...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Portland Press Ltd.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8128101/ https://www.ncbi.nlm.nih.gov/pubmed/33904577 http://dx.doi.org/10.1042/BSR20210029 |
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author | Matthews, Jennifer Villescas, Sofia Herat, Lakshini Schlaich, Markus Matthews, Vance |
author_facet | Matthews, Jennifer Villescas, Sofia Herat, Lakshini Schlaich, Markus Matthews, Vance |
author_sort | Matthews, Jennifer |
collection | PubMed |
description | In this review, we focus specifically on the role that the metalloproteinase, A Disintegrin and Metalloproteinase 17 [ADAM17] plays in the development and progression of the metabolic syndrome. There is a well-recognised link between the ADAM17 substrate tumour necrosis factor α (TNF-α) and obesity, inflammation and diabetes. In addition, knocking out ADAM17 in mice leads to an extremely lean phenotype. Importantly, ADAM17-deficient mice exhibit one of the most pronounced examples of hypermetabolism in rodents to date. It is vital to further understand the mechanistic role that ADAM17 plays in the metabolic syndrome. Such studies will demonstrate that ADAM17 is a valuable therapeutic target to treat obesity and diabetes. |
format | Online Article Text |
id | pubmed-8128101 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Portland Press Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-81281012021-05-25 Implications of ADAM17 activation for hyperglycaemia, obesity and type 2 diabetes Matthews, Jennifer Villescas, Sofia Herat, Lakshini Schlaich, Markus Matthews, Vance Biosci Rep Metabolism In this review, we focus specifically on the role that the metalloproteinase, A Disintegrin and Metalloproteinase 17 [ADAM17] plays in the development and progression of the metabolic syndrome. There is a well-recognised link between the ADAM17 substrate tumour necrosis factor α (TNF-α) and obesity, inflammation and diabetes. In addition, knocking out ADAM17 in mice leads to an extremely lean phenotype. Importantly, ADAM17-deficient mice exhibit one of the most pronounced examples of hypermetabolism in rodents to date. It is vital to further understand the mechanistic role that ADAM17 plays in the metabolic syndrome. Such studies will demonstrate that ADAM17 is a valuable therapeutic target to treat obesity and diabetes. Portland Press Ltd. 2021-05-14 /pmc/articles/PMC8128101/ /pubmed/33904577 http://dx.doi.org/10.1042/BSR20210029 Text en © 2021 The Author(s). https://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Metabolism Matthews, Jennifer Villescas, Sofia Herat, Lakshini Schlaich, Markus Matthews, Vance Implications of ADAM17 activation for hyperglycaemia, obesity and type 2 diabetes |
title | Implications of ADAM17 activation for hyperglycaemia, obesity and type 2 diabetes |
title_full | Implications of ADAM17 activation for hyperglycaemia, obesity and type 2 diabetes |
title_fullStr | Implications of ADAM17 activation for hyperglycaemia, obesity and type 2 diabetes |
title_full_unstemmed | Implications of ADAM17 activation for hyperglycaemia, obesity and type 2 diabetes |
title_short | Implications of ADAM17 activation for hyperglycaemia, obesity and type 2 diabetes |
title_sort | implications of adam17 activation for hyperglycaemia, obesity and type 2 diabetes |
topic | Metabolism |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8128101/ https://www.ncbi.nlm.nih.gov/pubmed/33904577 http://dx.doi.org/10.1042/BSR20210029 |
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